Microreviews – Page 8 – Microbial Cell

Microreviews, Review

Escherichia coli hijack Caspr1 receptor to invade cerebral vascular and neuronal hosts

Wei-Dong Zhao¹, Dong-Xin Liu¹, Yu-Hua Chen¹

In this article, the authors comment on the study "Caspr1 is a host receptor for meningitis-causing Escherichia coli" by Zhao et al. (Nat Commun, 2ß18) that identified Caspr1 as a key host receptor for E. coli virulence factor IbeA, facilitating E. coli penetration through the blood-brain barrier (BBB). The research demonstrated that targeting the interaction between IbeA and Caspr1 could potentially neutralize E. coli virulence and prevented meningitis, shedding light on the mechanisms of bacterial invasion into brain endothelial cells and hippocampal neurons.

A global view of substrate phosphorylation and dephosphorylation during budding yeast mitotic exit

Sandra A. Touati¹ and Frank Uhlmann¹

In this article, the authors comment on the study "Phosphoproteome dynamics during mitotic exit in budding yeast" by Touati (EMBO J, 2018) that described a time-resolved global phosphoproteome analysis during a cell cycle phase known as mitotic exit in budding yeast revealed the principles of phosphoregulation governing the ordered sequence of events such as spindle elongation, chromosome decondensation, and completion of cell division.

Gammaretroviruses tether to mitotic chromatin by directly binding nucleosomal histone proteins

Madushi Wanaguru¹ and Kate N. Bishop¹

In this article, the authors comment on the study "Murine leukemia virus p12 tethers the capsid-containing pre-integration complex to chromatin by binding directly to host nucleosomes in mitosis" by Wanaguruet al. (PLoS Pathog, 2018) that highlights the essential role of the gammaretroviral gag cleavage product, p12, at both early and late stages of the virus life cycle, particularly in the integration of the viral DNA into the host cell chromatin to form a provirus. It also emphasizes the recent findings regarding the N- and C-terminal domains of p12, revealing their direct binding to the viral capsid lattice and nucleosomal histone proteins, respectively, thus elucidating the mechanism by which p12 links the viral pre-integration complex to mitotic chromatin.

Methodologies for in vitro and in vivo evaluation of efficacy of antifungal and antibiofilm agents and surface coatings against fungal biofilms

Patrick Van Dijck^1,2,‡, Jelmer Sjollema^3,‡, Bruno P.A. Cammue^4,5, Katrien Lagrou^6,7, Judith Berman⁸, Christophe d’Enfert⁹, David R. Andes^10,11, Maiken C. Arendrup^12-14, Axel A. Brakhage¹⁵, Richard Calderone¹⁶, Emilia Cantón¹⁷, Tom Coenye^18,19, Paul Cos²⁰, Leah E. Cowen²¹, Mira Edgerton²², Ana Espinel-Ingroff²³, Scott G. Filler²⁴, Mahmoud Ghannoum²⁵, Neil A.R. Gow²⁶, Hubertus Haas²⁷, Mary Ann Jabra-Rizk²⁸, Elizabeth M. Johnson²⁹, Shawn R. Lockhart³⁰, Jose L. Lopez-Ribot³¹, Johan Maertens³², Carol A. Munro²⁶, Jeniel E. Nett³³, Clarissa J. Nobile³⁴, Michael A. Pfaller^35,36, Gordon Ramage^19,37, Dominique Sanglard³⁸, Maurizio Sanguinetti³⁹, Isabel Spriet⁴⁰, Paul E. Verweij⁴¹, Adilia Warris⁴², Joost Wauters⁴³, Michael R. Yeaman⁴⁴, Sebastian A.J. Zaat⁴⁵, Karin Thevissen^4,*

This article highlights the critical importance of accurate susceptibility testing methods and the discovery of novel antifungal and antibiofilm agents in combating invasive fungal infections associated with biofilm formation on medical devices, thereby emphasizing the need for advancements in medical mycology research to address these complex diseases.

Shepherding DNA ends: Rif1 protects telomeres and chromosome breaks

Gabriele A. Fontana¹, Julia K. Reinert^1,2, Nicolas H. Thomä¹, Ulrich Rass¹

This review discusses the conserved mechanisms cells have evolved to protect DNA ends at chromosomal termini and DNA double-strand breaks (DSBs), focusing on the protein Rif1’s roles in telomere homeostasis and DSB repair in eukaryotes. It highlights the intriguing connection between Rif1's involvement in both telomere maintenance and DSB repair, and suggests that excluding end-processing factors may underlie Rif1's diverse biological functions at telomeres and chromosome breaks.

The CRISPR conundrum: evolve and maybe die, or survive and risk stagnation

Jesús García-Martínez¹, Rafael D. Maldonado¹, Noemí M. Guzmán¹ and Francisco J. M. Mojica^1,2

In this article García-Martínez et al. cover how the model bacterium Escherichia coli deals with CRISPR-Cas to tackle the major dilemma of evolution versus survival.

A novel mechanism for regulation of the type I IFN response by herpesvirus deconjugases

Soham Gupta¹, Päivi Ylä-Anttila¹, Maria G. Masucci¹

In this article, the authors comment on the study "Herpesvirus deconjugases inhibit the IFN response by promoting TRIM25 autoubiquitination and functional inactivation of the RIG-I signalosome" by Gupta et al. (PLoS Pathog, 2018), discussing the finding of a novel mechanism for regulation of the type I IFN response by herpesvirus deconjugases.

Metabolic disharmony and sibling conflict mediated by T6SS

Vera Troselj¹ and Daniel Wall¹

In this article, the authors comment on the study "Physiological Heterogeneity Triggers Sibling Conflict Mediated by the Type VI Secretion System in an Aggregative Multicellular Bacterium" by Troselj et al. (MBio, 2018) discussing that M. xanthus uses T6SS to eliminate less fit cells from their population and identified toxic effector and cognate immunity protein (TsxEI) that mediates this sibling antagonism.

Helicobacter hepaticus polysaccharide induces an anti-inflammatory response in intestinal macrophages

Camille Danne¹ and Fiona Powrie¹

In this article, the authors comment on the study "A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages. " by Danne et al, (Cell Host Microbe 2017), discussing the interactions between H. hepaticus and intestinal macrophages that promote mutualism.

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Toxin-mediated gene regulatory mechanism in Staphylococcus aureus

December 29, 2016

This article comments on work published by Joo et al. (MBio, 2016), which describes the first molecular regulatory mechanism exerted by an S. aureus toxin, setting a paradigmatic example of how S. aureus toxins may influence cell functions to adjust them to times of toxin production.

NprR, a moonlighting quorum sensor shifting from a phosphatase activity to a transcriptional activator

November 5, 2016

This article comments on work published by Perchat et al. (PLoS Pathog, 2016), which demonstrates that, in the absence of the signaling peptide NprX, the sensor NprR is a dimer, which negatively controls sporulation in Bacillus thuringiensis, independently of its transcription factor activity.

The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency

November 4, 2016

This article comments on work published by Maroul et al. (PLoS Pathog, 2016), which demonstrates that the interaction of the viral genomes with the nuclear architecture and specifically the promyelocytic leukemia nuclear bodies is a major determinant for the entry of HSV-1 into latency.

Francisella IglG protein and the DUF4280 proteins: PAAR-like proteins in non-canonical Type VI secretion systems?

October 30, 2016

This article comments on work published by Rigard et al. (PLoS Pathog, 2013), which identified the function of IgIG, a protein of unknown function, encoded within the Francisella Pathogenicity Island.

B cell-helping functions of gut microbial metabolites

September 23, 2016

This article comments on work published by Kim et al. (Cell Host & Microbe, 2016), which showed that the microbial metabolites short-chain fatty acids (SCFAs) regulate the metabolism and gene expression in B cells to promote antibody production.

Cryptococcus flips its lid – membrane phospholipid asymmetry modulates antifungal drug resistance and virulence

August 1, 2016

This article comments on work published by Huang et al. (MBio, 2016), which reported that in the pathogenic fungus Cryptococcus neoformans loss of lipid flippase activity sensitized cryptococcal cells to multiple classes of antifungal drugs and abolished fungal virulence in murine models.